Respiratory Flashcards

1
Q

COPD

Pathophysiology

A
  • Non-reversible, long-term deterioration in air flow in the lungs
  • Damage to lung tissue → obstruction of air flow → more difficult to ventilation lungs → more prone to infections
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2
Q

COPD

Causes

A
  • Smoking!
  • Alpha-1-antitrypsin deficiency
  • Cadmium
  • Coal
  • Cotton
  • Cement
  • Grain
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3
Q

COPD

Features

A
  • Cough - often productive
  • Dyspnoea
  • Wheeze
  • Recurrent respiratory infections
  • Severe cases: RHF → peripheral oedema
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4
Q

COPD

how to quantify breathlessness?

A

MRC dyspnoea scale

  • Grade 1 = breathless on strenuous exercise
  • Grade 2 - breathless on walking up hill
  • Grade 3 - breathless that slows walking on the flat
  • Grade 4 - stop to catch their breath after walking 100 meters on the flat
  • Grade 5 - unable to leave house due to breathlessness
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5
Q

COPD

Investigations

A

Clinical presentation and spirometry!

Spirometry:
- FEV1/FVC ratio < 70%

CXR:
- Hyperinflation, bullae, flat hemidiaphragm

High res CT scan:
- Emphysema/chronic airway disease

Others:
- ECG, echo, sputum, alpha1AT, FBC, BMI, TLCO

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6
Q

COPD

Severity

A

All with post-bronch FEV1/FVC < 0.7

FEV1 (% predicted):

  • Stage 1 (Mild): > 80% (+ symptoms)
  • Stage 2 (Mod): 50-79%
  • Stage 3 (Severe): 30-49%
  • Stage 4 (Very severe): < 30%
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7
Q

COPD

General management

A
  • Smoking cessation - offer nicotine replacement therapy
  • Vaccines = one-off pneumococcal and annual flu vaccines
  • Pulmonary rehabilitation - start early, as soon as feeling breathless with regular activity
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8
Q

COPD

Medications

A
  • SABA or SAMA

If asthmatic features:

  • SABA/SAMA + LABA + ICS
  • Then triple therapy (remove SAMA if add LAMA)

If no asthmatic features:

  • SABA + LABA + LAMA
  • Then triple therapy (+ ICS)
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9
Q

COPD

What are the asthmatic features

A
  • Any previous, secure diagnosis of asthma or atopy
  • Higher blood eosinophil count
  • Substantial variation in FEV1 over time (≥ 400 ml)
  • Substantial diurnal variation in peak expiratory flow (≥ 20%)
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10
Q

COPD

Oxygen therapy

A
  • If retaining COaim for oxygen saturations of88-92%titrated byventuri mask - start with 28%
  • If not retaining COand their bicarbonate is normal (meaning they do not normally retain CO) then give oxygen to aim for oxygen saturations> 94%
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11
Q

COPD

Complications

A
  • Polycythaemia

- Cor Pulmonale

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12
Q

COPD

Factors that improve survival

A
  • Smoking cessation
  • LTOT
  • Lung volume reduction surgery in selected patients
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13
Q

COPD

Exacerbation
Features

A
  • Increase in dyspnoea, cough, wheeze
  • May be increased in sputum suggestive of infective cause
  • May be hypoxic and in some cases, have acute confusion
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14
Q

COPD

Exacerbation
Causative bacterial organisms

A
  • Haemophilus influenzae (most common)
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
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15
Q

COPD

Exacerbation
most common viral cause

A
  • Human rhinovirus
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16
Q

COPD

Exacerbation
Management

A
  • Increase frequency of bronchodilator
  • 30 mg Prednisolone PO for 5 days
  • Nebulisers
  • Abx only if sputum is purulent or there are clinical signs of pneumonia
    • Amoxicillin, Clarithromycin or Doxycycline
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17
Q

Lung cancer

Types

A

NSCLC (80%)

  • Adenocarcinoma
  • Squamous cell carcinoma
  • Large-cell carcinoma

SCLC (20%)
- Contain neurosecretory granules that can release neuroendocrine hormones –> responsible for many paraneoplastic syndrome

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18
Q

Lung cancer

Features

A
  • Persistent cough
  • Haemoptysis
  • Dyspnoea
  • Chest pain
  • Weight loss/anaemia
  • Recurrent pneumonia
  • Hoarseness (pancoast tumour on recurrent laryngeal nerve)
  • Superior vena cava syndrome
  • Fixed, monophonic wheeze
  • Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
  • Clubbing
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19
Q

Lung cancer

Investigations

A
  • 1st line = CXR
  • Staging CT scan
  • Bronchoscopy with biopsy
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20
Q

Lung cancer

Referral

A

2-week wait referral

  • CXR findings that suggest lung cancer
  • > 40 yrs with unexplained haemoptysis

OFFER urgent CXR (within 2 weeks):

  • > 40 yrs with 2 or more of following unexplained symptoms, or ever smoked and 1 of the following unexplained symptoms:
    • Cough
    • Fatigue
    • SOB
    • Chest pain
    • Weight loss
    • Appetite loss

CONSIDER urgent CXR (within 2 weeks):

  • > 40 yrs with any of following:
    • Persistent or recurrent chest infection
    • Clubbing
    • Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
    • Chest signs consistent with lung cancer
    • Thrombocytosis
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21
Q

Lung cancer

Management
NSCLC

A
  • Surgery if possible (lobectomy)
  • Mediastinopathy prior to surgery to show lymph node involvement
  • Curative or palliative radiotherapy
  • Poor response to chemo
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22
Q

Lung cancer

Management
SCLC

A
  • Surgery if early disease (T1-2a, N0, M0)
  • Combination of chemo and radiotherapy
  • Poorer prognosis than NSCLC
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23
Q

Pneumonia

Features
3 features on auscultation?

A
  • Productive cough
  • Chest pain - may be pleuritic
  • Dyspnoea
  • Fever
  • Tachycardia
  • Reduced O2 saturations
  • Auscultation:
    • Reduced breath sounds
    • Bronchial breathing
    • Focal coarse crackles
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24
Q

Pneumonia

Causes

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Mycoplasma pneumoniae
  • Legionella pneumophilia
  • Klebsiella pneumoniae
  • Pneumocystis jiroveci
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25
Pneumonia HAP time frame?
Develops > 48 hrs after admission and within 2 weeks of discharge
26
Pneumonia Investigations
- Sputum culture - Bloods - raised inflammatory markers, U&Es for urea for CURB65 - ABG if low sats/COPD - CXR - consolidation - Atypicals antigen testing
27
Pneumonia CURB-65 and scores
``` Confusion (< 8/10) Urea > 7mmol/L R: RR > 30 B: BP < 90mmHg systolic or 60 mmHg diastolic 65: > 65 yrs ``` 0-1: Home treatment 1-2: Hospital treatment 3+: Consider intensive care
28
Pneumonia Management
Mild: - 5 day course of PO Amoxicillin (or macrolide) Mod-Sev: - 7-10 day course of dual Abx therapy - Amoxicillin and a macrolide Repeat CXR at 6 weeks
29
Pneumonia Complications
- Sepsis - Pleural effusion - Empyema - Lung abscess - Death
30
Pneumonia S. pneumoniae
- 80% of pneumonia cases - High fever, rapid onset - Herpes labialis (cold sores!)
31
Pneumonia H. influenza
- Particularly common in COPD patients
32
Pneumonia S. aureus
- Often in patients with influenza infection or CF
33
Pneumonia Mycoplasma pneumoniae
- Atypical - Dry cough, atypical chest signs/XR findings - Autoimmune haemolytic anaemia - Erythema multiforme
34
Pneumonia Legionella pneumophilia
- Atypical pneumonia - Hyponatraemia - Lymphopenia - Air conditioning units (recent cheap holiday)
35
Pneumonia Klebsiella pneumonia
- Classically in alcoholics
36
Pneumonia Pneumocystis jiroveci
- FUNGAL - HIV - Dry cough - Exercise-induced desaturations - Absence of chest signs - Treat with co-trimoxazole (Trimethoprim and sulfamethoxazole)
37
PE Features
- Tachypnoea - Chest pain - typically pleuritic - Dyspnoea - Haemoptysis - Tachycardia - May have fever Resp exam: - Clear chest or crackles
38
PE Risk factors
- Immbolity - Long haul flihgts - Recent surgery - Pregnancy - Hormone therapy with oestrogen - Malignancy - Polycythaemia - SLE - Thrombophilia
39
PE PERC criteria
All must be negative to rule out PE - Age > 50 - HR > 100 - O2 sats < 94% - Previous DVT or PE - Recent surgery or trauma in past 4 weeks - Haemoptysis - Unilateral leg swelling - Oestrogen use (e.g. HRT, contraceptives)
40
PE Wells Score
- Clinical signs and symptoms of DVT (3) - Alternative diagnosis is less likely (3) - HR > 100 bpm (1.5) - Immobilisation for > 3 days or surgery in past 4 weeks (1.5) - Previous DVT/PE (1.5) - Haemoptysis (1) - Malignancy (on treatment, treated in last 6 months, or palliative) (1)
41
PE Investigations following Wells Score
If PE likely (> 4 Wells): - CTPA - Anticoagulation in the meantime (DOAC) - if negative --> proximal leg vein USS if DVT suspected If PE unlikely (< 4 Wells): - D-Dimer - If positive --> CTPA - If negative --> PE unlikely, stop any anticoagulation Renal impairment --> use V/Q scan instead of CTPA
42
PE Other investigations
- ECG: S1Q3T3 - CXR: typically normal, use to rule out other pathology - ABG: sometimes respiratory alkalosis with low pO2
43
PE Management
- Anticoagulation with DOAC (unless renal impairment or antiphospholipid syndrome --> LMWH) - Provoked vs unprovoked: 3 months for provoked, 6 months for unprovoked, 6 months for active cancer - If haemodynamically unstable--> Thrombolysis (e.g. alteplase) - If repeat PEs despite adequate anticoagulation --> consider IVC filter
44
TB Pathophysiology
- Mycobacterium tuberculosis: rod-shaped, acid-fast bacilli - Macrophages engulf the TB bacteria but TB bacteria secretes enzymes to inhibit its own breakdown -> encapsulated within macrophage -> proliferates -> caseous necrosis -> Gohn Focus - Gohn Focus + hilar lymph nodes = Gohn Complex Can stay like this as latent TB, then may reactivate if immunocompromised or in older age
45
TB Types
- Primary: Gohn complex etc - Secondary: reactivation, mostly in apex, cavitating lesions - Systemic miliary TB - spread via vascular system to other areas of the body
46
TB Extra-pulmonary infection
- CNS (Tb meningitis) - Vertebral bodies (Pott's disease) - Cervical lymph nodes (scrofuloderma) - Cold abscesses - usually on the neck - Renal (sterile pyuria, WBCs in urine) - Adrenal glands (Addisons) - Liver (hepatitis) - Cutaneous TB
47
TB Features
- Fever - Night sweats - Weight loss - Haemoptysis
48
TB Investigations
CXR - Primary TB: patchy consolidation, pleural effusions, bilateral hilar lymphadenopathy - Reactivated TB: patchy or nodular consolidation with upper lobe cavitation - Disseminated miliary TB: millet seeds appearance Sputum smear - 3 specimen - Use hypertonic saline or bronchoscopy with lavage if not producing sputum - Ziehl Neelson stain -> red on blue background - Done on Lowenstein-Jensen growth medium Sputum culture - Gold-standard - Can assess drug sensitivities - Can take 1-3 weeks
49
TB bCG vaccine
- Intradermal infection of live attenuated TB - Do Mantoux test prior to the vaccine - only give if negative - Assess for immunosuppression/HIV - Offer to high risk: - Neonates born in areas with high rates, with relatives from countries with high rates, Fx - Unvaccinated children/young adults (<35yrs) with close contact - Unvaccinated children/young adults who have recently arrived from high risk country - Healthcare workers
50
TB Management of active TB
Initial 2 months: - Rifampicin - Isoniazid - Pyrazinamide - Ethambutol Further 4 months: - Rifampicin - Isoniazid PLUS Pyridoxine (Vit B6) for full 6 months
51
TB RIfampicin SEs
- Red and orange urine - Hepatitis - Liver enzyme inducer
52
TB Isoniazid SEs
- Peripheral neuropathy (Vit B6 helps) - Hepatitis - Liver enzyme inhibitor - Agranulocytosis
53
TB Pyrazinamide SEs
- Hyperuricaemia -> gout - Arthralgia and myalgia - Hepatitis
54
TB Ethambutol SEs
- Difficulty recognizing colours | - Check visual acuity before and during treatment
55
TB Management of meningeal TB
- Prolonged period of 12 months of treatment | - PLUS steroids
56
TB DOTS
- Directly observed therapy - 3 times a week - For those in certain groups, e.g. homeless people with active TB, likely to have poor concordance, all prisoners with active or latent TB
57
TB Risk factors for reactivation of TB
- Silicosis - Chronic renal failure - HIV - Solid organ transplantation with immuosuppression - IVDU - Anti-TNF treatment - Previous gastrectomy - Older age
58
TB Screening for latent TB
Mantoux test - Purified protein derivative (PPD) - tuberculin - Injected intradermally - Result read 3 days later - Positive = had TB infection at some point - False negative may be seen in miliary TB, sarcoidosis, HIV, lymphoma, very young age (< 6 months) Interferon-gamma blood test - Looks for evidence of previous TB infection - Used in mantoux positive or equivocal, people where tuberculin test may be falsely negative - If has BCG, does not show positive (a bonus) If either are positive -> CXR to look for active infection
59
TB Treatment of latent TB
- 3 months or 'RI' (+ pyridoxine) OR - 6 months of Isoniazid (+pyridoxine)
60
Spirometry Restrictive pattern
- Reduced FEV1 < 80% - Reduced FVC <80% - Normal FEV1/FVC ratio >0.7/75% - Reduced TLCO
61
Spirometry Obstructive pattern
- Reduced FEV1 < 80% - Reduced FVC (but to a lesser extent than FEV1) - Reduced FEV1/FVC ratio <0.7/75%
62
Spirometry definitions
- FEV1: forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration - FVC: forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration
63
Spirometry graphs
- Obstructive: more gradual upwards trajectory, less flat | - Restrictive: same shape of trajectory but lower on the graph
64
Interstitial lung disease Definition
Umbrella term to describe conditions affecting the lung parenchyma Fibrosis --> replacement of normal elastic and functional lung tissue with scar tissue that is stiff and does not function as effectively
65
Interstitial lung disease Upper lobe diseases
CHARTS ``` Coal workers pneumonia Histiocytosis/Hypersensitivity pneumonitis Ankylosing spondylitis Radiation Tuberculosis Silicosis/sarcoidosis ```
66
Interstitial lung disease Lower lobe diseases
ICDA Idiopathic pulmonary fibrosis Connective tissue disorders, e.g. SLE Drug-induced: amiodarone, bleomycin, methotrexate Asbestosis
67
Interstitial lung disease Diagnosis
- CXR: ground glass changes | - Lung biopsy
68
Interstitial lung disease Management
- Remove/treat the underlying cause - Home oxygen is hypoxic at rest - Stop smoking - Physio and pulmonary rehabilitation - Flu and pneumococcal vaccines - Advanced care planning - Lung transplant - weigh up risks vs benefits
69
Idiopathic pulmonary fibrosis Epidemiology
- 50 - 70 yrs | - Twice as common in men
70
Idiopathic pulmonary fibrosis Features
- Insidious onset of SOB, dry cough > 3 months | - Bibasal fine inspiratory crackles and clubbing
71
Idiopathic pulmonary fibrosis Investigations
- Spirometry: restrictive picture - Reduced TLCO - High resolution CT = needed for diagnosis - CXR Ground glass changes and honeycombing
72
Idiopathic pulmonary fibrosis Management
- Pulmonary rehabilitation - Supplementary O2 - May need lung transplant eventually - Pirfenidone or Nintedanib may be used
73
Idiopathic pulmonary fibrosis Prognosis
2-5 years
74
Drug causes of pulmonary fibrosis
- Amiodarone - Cyclophosphamide - Methotrexate - Nitrofurantoin - Bleomycin
75
What is the TLCO
Total gas transfer! The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion.
76
What is KCO
TLCO that is corrected for lung volume
77
What might cause a high KCO and normal/reduced TLCO?
- Pneumonectomy/lobectomy - Scoliosis/kyphosis - Neuromuscular weakness - Ankylosis of costovertebral joints, e.g. ankylosing spondylitis
78
Causes of raised TLCO
- Asthma - Pulmonary haemorrhage (Wegener's, Goodpasture's) - L->R cardiac shunts - Polycythaemia - Hyperkinetic states - Male gender - Exercise
79
Causes of reduced TLCO
- Pulmonary fibrosis - Pneumonia - Pulmonary emboli - Pulmonary oedema - Emphysema - Anaemia - Low cardiac output
80
Secondary pulmonary fibrosis Causes
- Alpha-1 antitripsin deficiency - Rheumatoid arthritis - Systemic lupus erythematosus (SLE) - Systemic sclerosis
81
Extrinsic allergic alveolitis / Hypersensitivity pneumonitis Pathophysiology
- Hypersensitivity induced lung damage due to inhaled organic particles - Largely caused by immune-complex mediate tissue damage (type III hypersensitivity)
82
Extrinsic allergic alveolitis / Hypersensitivity pneumonitis Examples
- Birds fancier lungs (avian proteins from bird droppings, chlamydia psittaci) - Farmers lung (spores of saccharopolyspora rectivirgula from wet hay) - Malt workers lung (aspergillus clavatus) - Mushroom workers' lung (thermophilic actinomycetes)
83
Cryptogenic Organising Pneumonia What Dx Tx
What? - Focal area of inflammation of the lung tissue Dx: - Present similarly to pneumonia - Lung biopsy is definitive Ix Tx - Systemic corticosteroids
84
Asbestosis Pathophysiology
- Inhalation of asbestos - Fibrogenic to lungs - Oncogenic too - Effects usually take decades to develop
85
Asbestosis Features
- Pleural plaques (benign, do not undergo malignant change, do not require follow up, occur after latent phase 20-40yrs) - Pleural thickening - Lung fibrosis - Asbestosis (severity is linked to length of exposure, latent period 15-30 yrs, lower lobe, SOB and reduced exercise tolerance) - Adenocarcinoma - Mesothelioma (malignant disease)
86
Mesothelioma Which asbestos is most dangerous?
Crocidolite (blue)
87
Mesothelioma Features
- Progressive SOB - Chest wall pain - Pleural effusion (generally painless) - Clubbing - Weight loss - Hx of asbestos exposure in 85-90% (latent period of 30-40 years)
88
Mesothelioma Tx
- Palliative chemo - Limited role for surgery/radiotherapy - Industrial compensation
89
Mesothelioma Prognosis
Poor 8-14 months = median survival
90
Pleural effusion Transudate causes
< 30 g/L - Heart failure (most common transudate cause) - Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption) - Hypothyroidism - Meig's syndrome - Kidney failure/nephrotic syndrome
91
Pleural effusion Exudate causes
> 30 g/L - Infection: Pneumonia (most common exudate cause), TB, subphrenic abscess - Connective tissue disease (RA, SLE) - Neoplasia (lung cancer, mesothelioma, metastases) - Pancreatitis - Pulmonary embolism - Dressler's syndrome - Yellow nail syndrome
92
Pleural effusion Light's criteria
If the protein level is between 25-35 g/L, Light's criteria An exudate is likely if at least one of the following criteria are met: - Pleural fluid protein divided by serum protein >0.5 - Pleural fluid LDH divided by serum LDH >0.6 - Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
93
Pleural effusion Other characteristic pleural fluid findings
- Low glucose: rheumatoid arthritis, tuberculosis - Raised amylase: pancreatitis, oesophageal perforation - Heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis
94
Pleural effusion Features
- Dyspnoea - Non-productive cough - Chest pain - Dullness to percussion - Reduced breath sounds - Reduced chest expansion
95
Pleural effusion Imaging
- PA chest X-Ray - USS - Contrast CT - Aspiration
96
Pleural effusion Aspiration
- As above, ultrasound is recommended to reduce the complication rate - A 21G needle and 50ml syringe should be used - Fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
97
Pleural effusion Management
- Depends on the cause, e.g. HF -> diuretics, Infection -> Abx - Recurrent aspiration - Pleurodesis - Indwelling pleural catheter - Drug management to alleviate symptoms, e.g. opioids to relieve dyspnoea
98
Pleural effusion CXR findings
- Blunting of the costophrenic angle - Fluid in the lung fissures - Larger effusions will have a meniscus. This is a curving upwards where it meets the chest wall and mediastinum. - Tracheal and mediastinal deviation if it is a massive effusion
99
Empyema Define
Empyema is where there is an infected pleural effusion.
100
Empyema When to suspect?
Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever
101
Empyema Investigations
Pleural aspiration shows pus, acidic pH (pH < 7.2), low glucose and high LDH
102
Empyema Management
Empyema is treated by chest drain to remove the pus and antibiotics
103
Bronchiectasis Causes
- Post-infective: TB, measles, pertussis, pneumonia - Cystic fibrosis - Bronchial obstruction: lung cancer/foreign body - Immune deficiency: selective IgA, hypogammaglobulinemia - Allergic bronchopulmonary aspergillosis (ABPA) - Ciliary dyskinetic syndromes: Kartagener's syndrome, Young's syndrome - Yellow nail syndrome
104
Bronchiectasis Organisms
- Haemophilus influenzae (most common) - Pseudomonas aeruginosa - Klebsiella spp. - Streptococcus pneumoniae
105
Bronchiectasis Features
- Persistent cough - Copious purulent sputum - Intermittent haemoptysis - SOB - Recurrent chest infections - Clubbing - Coarse inspiratory crepitations
106
Bronchiectasis Investigations
- Sputum culture - CXR: dilated bronchi, ring/cystic shadows, tram-tracks - High resolution CT: tram-tracks, wide bronchi, signet ring signs
107
Bronchiectasis Management
- Physical training - Postural drainage - Abx for exacerbations and long-term rotating Abx in severe cases - bronchodilators - Immunisations - Surgery in selected cases (e.g. localised disease)
108
Bronchiectasis Pathophysiology
Permanent dilatation of the airways secondary to chronic infection or inflammation
109
LTOT in COPD
LTOT should be offered to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following: - Secondary polycythaemia - Nocturnal hypoxaemia - Peripheral oedema - Pulmonary hypertension
110
Azithromycin in COPD Criteria
- Not smoker - Optimised standard treatment - Continue to have exacerbations
111
Azithromycin in COPD Prior to starting tx
- CT thorax (exclude bronchiectasis) - Sputum culture (exclude atypical infections and TB) - LFTs - ECG to exclude QT prolongation
112
Acute respiratory distress syndrome Causes
- Infection - Massive blood transfusion - Trauma - Smoke inhalation - Acute pancreatitis - Cardio-pulmonary bypass
113
Acute respiratory distress syndrome Features
- Acute onset (within 1 week of known RF) - Dyspnoea - Elevated RR - Bilateral lung crackles - Low O2 sats
114
Acute respiratory distress syndrome Investigations
- ABG - CXR: bilateral infiltrates (pulmonary oedema) - Non-cardiogenic (pulmonary artery wedge pressure needed if doubt) - pO2/FiO2 < 40 kPa (200 mmHg)
115
Acute respiratory distress syndrome Management
- ITU - Oxygenation/ventilation to treat hypoxaemia - General organ support (e.g. vasopressors) - Tx of underlying cause - Prone positioning and muscle relaxation
116
Asthma Stepdown therapy
In the step-down treatment of asthma, aim for a reduction of 25-50% in the dose of inhaled corticosteroids
117
Extrinsic allergic alveolitis Features
Acute (4-8 hrs after exposure): - Dyspnoea - Dry cough - Fever Chronic (weeks-months): - Weight loss - Productive cough - Dyspnoea - Lethargy
118
Extrinsic allergic alveolitis Investigations
- Imaging: upper/mid-zone fibrosis - Bronchoalveolar lavage: lymphocytosis - Serologic assays for specific IgGs - Blood: NO eosinophilia
119
Extrinsic allergic alveolitis Management
- Avoid triggers | - Oral glucocorticoids for severe cases or failure to avoid triggers
120
Kartagener's syndrome Features
- Dextrocardia or complete situs inversus - Bronchiectasis - Recurrent sinusitis - Subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
121
Kartagener's syndrome Pathophysiology
- Primary ciliary dyskinesia - Dextrocardia = quiet heart sounds, small volume complexes in lateral leads - Dynein arm defect results in immotile cilia
122
Lung cancer Small cell Paraneoplastic features
SIADH - Hyponatraemia ACTH (not typical) - Hypertension - Hyperglycaemia - Hypokalaemia - Alkalosis - Muscle weakness - CUSHINGS Lambert-Eaton Syndrome
123
Lung cancer Squamous cell Paraneoplastic features
- Hypercalcaemia - Clubbing - Hypertrophic pulmonary osteoarthropathy (HPOA) - Hyperthyroidism due to ectopic TSH
124
Lung cancer Adenocarcinoma Paraneoplastic features
- Gynaecomastia | - Hypertrophic pulmonary osteoarthropathy (HPOA)
125
Pneumothorax Features
RAPID onset - Dyspnoea - Chest pain - pleuritic - Sweating - Tachypnoea - Tachycardia
126
Pneumothorax Risk factors
- Pre-existing lung disease (COPD/asthma/CF/lung cancer/pneumocystis pneumonia) - Connective tissue disease (Marfans/RA) - Ventilation! - Catamenial pneumothorax (related to menstruation)
127
Pneumothorax Types
- Primary: no underlying lung disease | - Secondary: underlying lung disease present
128
Pneumothorax Tx of primary pneumothorax
- If rim of air < 2cm and no SOB -> consider discharge - Otherwise ASPIRATION - If this fails (> 2cm still or SOB) then chest drain
129
Pneumothorax Tx of secondary pneumothorax
- If > 50 yrs and rim of air > 2cm +/- SOB then CHEST DRAIN - Otherwise ASPIRATION - If < 1cm then O2 and admit for 24 hrs
130
Pneumothorax Iatrogenic Tx
- Less likely to recurs than spontaenous - Majority resolve with observation - Aspiration if Tx required - If COPD/ventilation, may consider a chest drain
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Pneumothorax Discharge advise
- NEVER scuba dive - No travel by air for 1 week post check XR - Avoid smoking to reduce risk of further episodes
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Obstructive sleep apnoea Predisposing factors
- Obesity - Macroglossia: acromegaly, hypothyroidism, amyloidosis - Large tonsils - Marfan's syndrome
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Obstructive sleep apnoea Consequences
- Snoring - Period of apnoea - Daytime somnolence - Compensated respiratory acidosis - HYPERTENSION
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Obstructive sleep apnoea Assessment of sleepiness
- Epworth sleepiness scale | - Multiple Sleep Latency Test (MSLT) - measures time to fall asleep in a dark room
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Obstructive sleep apnoea Diagnostic tests
Sleep studies (polysomnography) - Ranging from monitoring of pulse oximetry at night to full polysomnography - Full includes: EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry
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Obstructive sleep apnoea Management
- Weight loss - CPAP = 1st line for moderate-severe - Intra-oral devices (e.g. mandibular advancement) if CPAP not tolerated or mild OSAHS with no daytime sleepiness - DVLA should be informed if excessive daytime sleepiness
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Causes of haemoptysis
- Lung cancer - Pulmonary oedema - TB - PE - LRTI - Bronchiectasis - Mitral stenosis - Aspergilloma - Granulomatosis with polyangiitis - Goodpasture's syndrome
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Aspergilloma Pathophysiology
- Mass-like fungus ball (mycetoma) | - Colonises an existing lung cavity (e.g. secondary to malignancy, TB, CF)
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Aspergilloma Features
- Usually asymptomatic - Cough - Haemoptysis
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Aspergilloma Investigations
- CXR: round opacity | - High titres Aspergillus precipitins
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Acute bronchitis Pathophysiology
- Self-limiting chest infection - Result of inflammation of trachea and major bronchi - Oedematous large airways and production of sputum
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Acute bronchitis Features
- Cough - Sore throat - Rhinorrhoea - Wheeze - Sometimes low-grade fever
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Acute bronchitis Differentiating from pneumonia
- Hx: sputum, wheeze, breathlessness may be absent in acute bronchitis - Examination: only wheeze in acute bronchitis. In pneumonia would see dullness to percussion, creps, bronchial breathing
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Acute bronchitis Investigations
- Typically a clinical diagnosis | - CRP can guide the need for Abx
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Acute bronchitis Management
- Analgesia - Good fluid intake Consider Abx therapy if: - Systemically very unwell - Pre-existing co-morbidities - CRP of 20-100 (delayed prescription) or > 100 (immediately) - Doxy would be 1st line if Abx needed. NOT in children/pregnancy -> Amoxicillin.
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Acute asthma Moderate
- PEFR 50-75% best or predicted - Normal speech - RR < 25 - HR < 110
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Acute asthma Severe
- PEFR 33-50% - Can't complete sentences - RR > 25 - HR > 110
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Acute asthma Life-threatening
- PEFR < 33% - O2 sats < 92% - Silent chest - Cyanosis - Feeble resp effort - Bradycardia - Dysrhythmia - Hypotension - Exhaustion - Confusion - Coma - NORMAL CO2 = EXHAUSTION
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Sarcoidosis Indications for steroids
- CXR stage 2 or 3 disease AND symptomatic - Hypercalcaemia - Eye. heart and neuro involvement
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Sarcoidosis Features
Acute: - Erythema nodosum - Bilateral hilar lymphadenopathy - Swinging fever - Polyarthralgia Insidious: - Dyspnoea - Non-productive cough - Malaise - Weight loss Skin: - Lupus pernio Hypercalcaemia: - Macrophages inside the granulomas cause increased conversion of Vit D to 1, 25-dihydroxycholecalciferol
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Sarcoidosis Pathophysiology
- Mutilsystem disorder | - Non-caseating granulomas
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Sarcoidosis Epidemiology
More common in - Young adults - African descent
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Asbestosis Ethics
- Suffers are eligible for compensation if they develop asbestos related health conditions (except isolated pleural plaques). - All patients that die with known exposure to asbestos need to be referred to the coroners.
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Mesothelioma Pathophysiology
- Malignancy of mesothelial cells of pleura - Metastases to contralateral lung and peritoneum - Right lung affected more often than left
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Mesothelioma Investigations
- CXR: pleural effusions or pleural thickening If pleural effusion -> send for MC&S, biochemistry and cytology - Pleural CT - Local anaesthetic thoracoscopy - Image-guided pleural biopsy if pleural nodularity seen on CT
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Pulmonary hypertension Pathophysiology
- Increased resistance and pressure of blood in pulmonary arteries - Causes strain on the right side of the heart - Back pressure of blood into systemic venous system
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Pulmonary hypertension Causes
5 groups - Group 1: Primary pulmonary hypertension or connective tissue disease (e.g. SLE) - Group 2: LHF - usually due to MI/systemic HTN - Group 3: Chronic lung disease (e.g. COPD) - Group 4: Pulmonary vascular diseases (e.g. PE) - Group 5: Misc, e,g, sarcoidosis, glycogen storage disease, haematological disorders
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Pulmonary hypertension Features
- SOB - Syncope - Raised JVP - Hepatomegaly - Peripheral oedema
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Pulmonary hypertension Investigations
- ECG: RH strain - R ventricular hypertrophy, right axis deviation, RBBB - CXR: Dilated pulmonary arteries, right ventricular hypertrophy - Others: Raised NT-proBNP (RVF), Echo to estimate pulmonary artery pressure
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Pulmonary hypertension Management
Primary: - IV prostanoids (e.g. epoprostenol) - Endothelin receptor antagonists (e.g. macitentan) - Phosphodiesterase-5-inhibitors (e.g. sildenafil) Secondary: - Treat underlying cause Supportive treatment for resp failure, arrhythmias, HF
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Goodpasture's Syndrome / Anti-glomerular basement membrane (GBM) disease Epidemiology
- More common in men - Bimodal age distribution (20-30 yrs and 60-70 yrs) - Associated with HLA DR2
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Goodpasture's Syndrome / Anti-glomerular basement membrane (GBM) disease Features
- Pulmonary haemorrhage | - Rapidly progressive glomerulonephritis
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Goodpasture's Syndrome / Anti-glomerular basement membrane (GBM) disease Investigations
- Renal biopsy: linear IgG deposits along basement membrane, crescentic glomerulonephritis - Raised transfer factor, secondary to pulmonary haemorrhages - Anti-GBM antibodies
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Goodpasture's Syndrome / Anti-glomerular basement membrane (GBM) disease Management
- Plasma exchange (plasmapheresis) - Steroids - Cyclophophamide
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Factors that increase the likelihood of pulmonary haemorrhage
- Smoking - Lower respiratory tract infection - Pulmonary oedema - Inhalation of hydrocarbons - Young males
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Granulomatosis with polyangiitis (Wegener's) Features
- URT: epistaxis, sinusitis, nasal crusting - LRT: dyspnoea, haemoptysis - Rapidly progressive glomerulonephritis - Saddle-shaped nose - Vasculitis rash - Eye involvement - Cranial nerve lesions
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Granulomatosis with polyangiitis (Wegener's) Investigations
- Renal biopsy: epithelial crescents in Bowman's capsule - CXR: cavitating lesions - cANCA (90%) - pANCA (25%)
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Acute asthma Features
- Progressively worsening SOB - Use of accessory muscles - Tachypnoea - Symmetrical expiratory wheeze on auscultation - Tight chest, reduced air entry
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Acute asthma Near fatal asthma
- High CO2 (respiratory acidosis) | - Mechanical ventilation requirement
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Acute asthma Management
O SHIT ME ``` O: Oxygen S: Salbutamol nebs H: Hydrocortisone/Pred for 5 days I: Ipratropium bromide nebs T: Theophylline/aminophylline (severe) M: Magnesium sulphate (LT) E: Escalate - HDU/ITU/intubation (LT) ```
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Acute asthma Monitoring response
- Respiratory rate - Respiratory effort - Peak flow - Oxygen saturations - Chest auscultation - Monitor serum potassium when on salbutamol
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Acute asthma Admission criteria
- Life-threatening acute attack - Severe and not responding to initial treatment - Previous near-fatal asthma attack
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Acute asthma Criteria for discharge
- Been stable on their discharge medication (i.e. no nebulizers or oxygen) for **12–24 hours** - **Inhaler technique** checked and recorded - Check compliance with meds - **PEF >75%** of best or predicted - Asthma action plan and possible rescue pack - Referral to a respiratory specialist if > 2 attacks in 12 months
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Chronic asthma Pathophysiology
- Causes episodic exacerbations of bronchoconstriction - A reversible airway obstruction - Responds to bronchodilators, e.g. Salbutamol - Caused by Type I hypersensitivity
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Chronic asthma Common triggers (7)
- Infection - Night time or early morning - Exercise - Animals - Cold/damp - Dust - Strong emotions
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Chronic asthma Risk factors (9)
- Personal/family Hx of atopy - Antenatal factors: maternal smoking, viral infection during pregnancy (especially RSV) - Low birth weight - Not being breastfed - Maternal smoking - Exposure to high concentrations of allergens (e.g. house dust mite) - Air pollution - Hygiene hypothesis - Occupation
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Chronic asthma Presentation
- Episodic symptoms - Diurnal variability, typically **worse at night** - Dry cough with wheeze and SOB - Hx of atopic conditions, such as eczema, hayfever and food allergies - Family Hx - Bilateral widespread expiratory polyphonic wheeze - A number of patients with asthma are sensitive to aspirin. Patients who are most sensitive to asthma often suffer from nasal polyps (Samter's triad).
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Chronic asthma Presentations that may indicate a diagnosis other than asthma
- Wheeze related to coughs and colds more suggestive of viral induced wheeze - Isolated or productive cough - Normal investigations - No response to treatment - Unilateral wheeze → suggests focal lesion of infection
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Chronic asthma Investigations
- 1st line = spirometry with bronchodilator reversibility and FeNO Spirometry: - Reduced FEV1, normal FVC, FEV1/FVC < 70% Reversibility: - FEV1 improve by 12% or increase in volume by 200 ml FeNO: - > 40 parts per billion Peak expiratory flow variability > 20%
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Chronic asthma Drug management
1. SABA 2. ICS 3. LABA or Montelukast 4. The one that wasn't added preivously 5. Maintenance and reliever therapy (MART): ICS and LABA combined
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Chronic asthma Stepping down treatment
- Consider stepping down treatment every 3 months or so | - When reducing inhaled steroids, do this by 25-50% at a time
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Chronic asthma Additional management
- Individual asthma self-management programme - Yearly flu jab - Yearly asthma review - Advise exercise and avoid smoking
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Occupational asthma Associations
- Isocyanates (spray painting/foam moulding) - Platinum salts - Soldering flux resin - Glutaraldehyde - Flour - Epoxy resins - Proteolytic enzymes
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Occupational asthma Diagnosis
- Serial peak flows when at work and away from work
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Occupational asthma Management
Referral to resp specialist
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Silicosis Pathophysiology
- Fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica) - It is a risk factor for developing TB (silica is toxic to macrophages)
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Silicosis Occupations at risk
- Mining - Slate works - Foundries - Potteries
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Silicosis Features
- Fibrosing lung disease | - 'Egg-shell' calcification of hilar lymph nodes
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Coal workers pneumoconiosis Pathophysiology
- Long term exposure to coal dust particles - Coal dust (2-5 nanometres) enters the lungs - Dust reaches terminal bronchioles and is engulfed by alveolar and interstitial macrophages - Moved by macrophages to mucociliary elevator and removed from body as mucus - In over exposure to coal dust -> system is overwhelmed -> macrophages accumulate in alveoli -> immune response -> damage to lung tissue
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Coal workers pneumoconiosis Epidemiology
- Higher in populations with higher levels fo exposure (many coal mines) - Severity linked to length of exposure - Male (likely due to prevalence in coal mines) - Makes up 7% of all pneumoconiosis - Diagnosis usually made 15-20 yrs after initial exposure
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Coal workers pneumoconiosis Simple penumoconiosis
- Most common type - Most are asymptomatic - Increases risk of lung disease, e.g. COPD - May lead to progressive massive fibrosis (PMF)
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Coal workers pneumoconiosis Staging
Category 1: some opacities but normal lung markings visible Category 2: large number of opacities but normal lung markings visible Category 3: large number of opacities with normal lung not visible
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Coal workers pneumoconiosis Investigations
- CXR: Upper zone fibrosis - Spirometry: Restrictive pattern A normal or slightly reduced FEV1 and a reduced FVC
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Coal workers pneumoconiosis Management
- Avoid exposure to coal dust and other resp irritants, e.g. smoking - Manage symptoms of chronic bronchitis - Patients eligible for compensation via Industrial Injuries Act
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What is a pneumoconiosis
Pneumoconiosis = accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal workers’ pneumoconiosis.
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Progressive Massive Fibrosis
- Dust exposure causes patients to develop round fibrotic masses which can be several centimeters in diameter - These are most commonly in the upper lobes. - The exact pathogenesis is not known. - Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum. - Lung function testing shows a mixed obstructive/restrictive picture.
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Signs of respiratory distress
- Raised respiratory rate - Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles - Intercostal and subcostal recessions - Nasal flaring - Head bobbing - Tracheal tugging - Cyanosis (due to low oxygen saturation) - Abnormal airway noises
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Bronchiolitis Epidemiology
- < 1 year, peak 3-6 months | - Very common in winter
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Bronchiolitis Who is it more severe in?
- Congenital heart problems - Downs syndrome - CF - Bronchopulmonary dysplasia (premature) - Dual infection with metapneumovirus
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Bronchiolitis Causative organisms
- **RSV (75-80%)** - Mycoplasma - Adenoviruses
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Bronchiolitis Presentation
- Coryzal symptom preceding - Dry cough - Wheeze - Respiratory distress signs - Fine end-inspiratory crackles - SOB - Feeding difficulties (children) - Mild fever - Apnoeas - Tachypnoea
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Bronchiolitis When to admit?
- If Downs/congenital heart disease/CF etc - < 3 months - RR > 70 bpm, head bobbing, grunting, recessions - Child looks seriously unwell to HCP - Apnoea - SpO2 < 92% - Central cyanosis
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Bronchiolitis Investigations
- Pulse oximetry - Viral throat swab - Nasopharyngeal secretion immunofluorescence may reveal RSV - If severe -> CXR, blood gas, FBC
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Bronchiolitis Management
- Most = self-limiting (peak 3-5 days) - Nasogastric feeding if cannot drink/eat - Suction if excessive secretions - Humidified O2 if sats < 92% - Maybe PEEP/CPAP - Intubation if required, monitor using cap blood gases - Poor ventilation = high CO2, falling pH - RIBAVIRIN → for immunocompromised and heart/lung conditions
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Bronchiolitis Prophylaxis
- Palivizumab = **monoclonal antibody** that targets RSV. Given as prophylactic monthly injection to high risk babies, such as **ex-premature** and those with **congenital heart disease** - Maternal IgG can protect newborns against RSV
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Cystic fibrosis Pathophyisology
- Autosomal recessive disorders - Causes increased viscosity of secretions (e.g. lungs and pancreas) - Due to defect in cystic fibrosis transmembrane conductance regulator gene (CFTR) which codes a cAMP-regulated chloride channel - In UK - 80% are due to delta F508 on long arm of chromosome 7 - Affects 1 per 2500 births - Carrier rate is 1 in 25 - Around 5% are diagnosed after 18yrs
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CF Consequences of mutation
- Thick pancreatic and biliary secretions → blockage of the ducts → lack of digestive enzymes such as pancreatic lipase in the digestive tract - Low volume thick airway secretions → reduce airway clearance → bacterial colonisation and susceptibility to airway infections - Congenital bilateral absence of the vas deferens in males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in **male infertility** - **Female subfertility**
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CF Organisms that may colonise
- S. aureus (prophylactic fluclox) - Pseudomonas aeruginosa (neb tobramycin) - Burkholderia cepacia - Aspergillus - Escherichia coli - Klebsiella pneumoniae - Haemophilus influenza
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CF Features
- Neonatal period: meconium ileus (abdo distension and vomiting), prolonged jaundice - Recurrent chest infections (40%) - Malabsorption (30%): steatorrhorea, failure to thrive - Liver disease, pancreatitis - Chronic cough - Thick sputum production - Salty taste when kissing (concentrated salt in sweat) - Delayed puberty - Rectal prolapse (due to bulky stools) - Diabetes mellitus - Short stature - Nasal polyps - Clubbing - Crackles and wheeze on auscultation - Male infertility, female subfertility
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CF Investigations
- Newborn blood spot test - Genetic testing for CFTR gene (amniocentesis, chorionic villous sampling) - Sweat test (> 60 mEq/L of Cl-)
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CF Causes of false-positive sweat test
- Malnutrition - Adrenal insufficiency - Glycogen stroage disease - Nephrogenic diabetes inspidus - Hypothyroidism, hypoparathyroidism - G6PD - Ectodermal dysplasia
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CF Cause of false-negative sweat test
Skin oedema, often due to hypoalbuminaemia / hypoproteinaemia secondary to pancreatic exocrine insufficiency
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CF Management
- Chest physiotherapy and postural drainage (>BD) - High calorie diet and high fat intake - Exercise - Minimise contact with each other to prevent cross infection with *Burkholderia cepacia* complex and *Pseudomonas aeruginosa* - Vitamin supplementation - Pancreatic enzyme supplements taken with meals (CREON tablets) - Bronchodilators (e.g. Salbutamol) can help treat bronchoconstriction - Nebulised DNase or hypertonic saline - Vaccinations: pneumococcal, influenza, varicella - Fertility treatment and genetic counselling Lung transplantation Lumacaftor/lvacaftor (Orkambi): - Used in CF patients who are homozygous for delta F508 mutation
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CF MoA of Ivacaftor
Potentiator of CFTR that is already at cell surface, increasing the probability that the defective channel with be open and allow chloride ions to pass through the channel pore
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Cf MoA of Lumacaftor
Increases CFTR protein numbers that are transported to cell surface
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CF Lung transplantation CI
Chronic infection with Burkholderia cepacia is an important CF-specific CI to lung transplantation
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CF Monitoring
- Followed up every 6 months - Regular monitoring of sputum for colonisation - Monitoring for DM, osteoporosis, Vit D deficiency, liver failure
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CF Prognosis
- 90% of patients with CF develop pancreatic insufficiency - 50% of adults with CF develop cystic fibrosis-related diabetes and require treatment with insulin - 30% of adults with CF develop liver disease - Most males are infertile due to absent vas deferens
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What are the boundaries of the 'safe triangle' for chest drain insertion?
- Anterior edge latissimus dorsi - Lateral border of pectoralis major - Line superior to the horizontal level of the nipple (5th intercostal space) - Apex below the axilla
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Causes of an anterior mediastinal mass?
4 T's - Teratoma - Terrible lymphadenopathy - Thymic mass - Thyroid mass